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Edaravone Dexborneol facilitates peripheral nerve regeneration through suppressing oxidative damage and autophagy flow |
CHEN Jinghao, LOU Chenghao, WEI Shengzhe, LU Yingfeng, YU Fangzheng, WANG Jian. |
1.Department of Wound Repair, the First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325015, China; 2.Department of Hand Surgery and Peripheral Neurosurgery, the First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325015, China; 3.School of Pharmaceutical Science, Wenzhou Medical University, Wenzhou 325035, China |
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Abstract Objective: To investigate the role of Edaravone Dexborneol (C-EDA) in regulating oxidative stress and autophagy flow in peripheral nerve injury (PNI). Methods: PNI model was established by moderate crush injury to the sciatic nerve with a vascular clamp. The rats were randomly divided into Sham group, PNI group, C-EDA group (C-EDA+PNI), and 3MA group [PNI+C-EDA+3MA (3-methyladenine)]. At the 4th week after operation, gait imprinting, neuroelectrophysiological detection, wet weight measurement of gastnemius muscle, HE staining of muscle tissue and NF-200+MBP immunofluorescence staining of nerve tissue were performed in all rats. The levels of oxidative stress-related proteins Nrf2 and HO-1, autophagy related proteins LC3 II/LC3 I and p62 (autophagy substrate protein, reflecting whether autophagy flow was unobstructed), apoptosisrelated proteins Bcl-2 and Bax were detected by Western blot. Results: Compared with the PNI group, C-EDA+ PNI improved the posterior foot deformity, improved nerve conduction function and reduced gastrocnemius atrophy. 3MA reversed the effect of C-EDA on improving neurological function after injury. Compared with PNI group, C-EDA up-regulated the expressions of oxidative stress-related proteins Nrf2, HO-1 and anti-apoptotic protein Bcl-2, and down-regulated the expressions of autophagy substrate protein p62 and pro-apoptotic protein Bax (P<0.05). Conclusion: Our study confirms that C-EDA can unobstruct autophagy flow, playing a role in improving neural structure repair and functional recovery after PNI. Therefore, it is a potentially effective method for the treatment of PNI.
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PENG Ziying, NAN Yan, XIE Xianhai, LI Xiaoxiao, GAO Ling, ZHANG Lei, YAO Ruina, YING Lei, WANG Yang. Fibroblast growth factor 1 alleviates acetaminophen-induced acute liver injury in mice via improving mitochondrial oxidative stress[J]. JOURNAL OF WEZHOU MEDICAL UNIVERSITY, 2023, 53(4): 259-268. |
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